ArticleAndrology2026
Slit2/Robo Signaling Restores Diabetic Erectile Function via Neurovascular Remodeling.
Article in Andrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDiabetes mellitus-induced erectile dysfunction (DMED) is a common and debilitating vascular-neurogenic complication of diabetes. The poor responsiveness of DMED patients to phosphodiesterase type-5 inhibitors underscores the need for therapies capable of restoring both endothelial integrity and cavernous nerve function. The Slit2/Roundabout (Robo) pathway, a conserved regulator of axon guidance and vascular remodeling, is well positioned to coordinate neurovascular repair; however, its involvement in DMED remains largely undefined.
methodsSingle-cell RNA sequencing from embryonic genital tubercle to postnatal stages was used to map fibroblast-endothelial-neuronal signaling and identify Slit2 as a key secreted ligand. Diabetic and control mouse corpus cavernosum tissues were analyzed for endothelial and neuronal Slit2-Robo1/4 activity. In vitro, recombinant Slit2-N was applied to cells under high glucose to assess proliferation, migration, tube/sprout formation, and neurite outgrowth; Robo1/4 knockdown tested receptor dependency. In vivo, AAV-Slit2 was delivered intracavernously to diabetic mice, with erectile function assessed by sodium-nitroprusside perfusion and electrostimulation, and structural remodeling evaluated by endothelial, neural, and fibrosis markers.
resultsSingle-cell profiling identified Slit2 as a fibroblast-derived developmental cue for corpus cavernosum morphogenesis. Diabetic mice exhibited markedly reduced endothelial and neuronal Slit2-Robo signaling. Slit2-N restored angiogenic and neuroregenerative functions in vitro under high glucose, enhancing endothelial activity and neurite growth; all effects were lost after Robo1/4 silencing. In vivo, AAV-Slit2 re-established local Slit2 signaling, improved penile perfusion and erectile responses, enhanced endothelial proliferation and nerve regeneration, and reduced fibrosis, indicating substantial neurovascular recovery.
conclusionsSlit2/Robo signaling is a key regulatory axis disrupted in DMED. Local restoration of Slit2 via AAV delivery drives synchronized neurovascular regeneration and effectively rescues erectile function in diabetic mice. These findings establish Slit2 as a promising therapeutic target for reversing the underlying pathophysiology of DMED rather than merely providing symptomatic relief.
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